Page 1342 - Veterinary Immunology, 10th Edition

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FIV binds specifically to CD134 expressed on a subset of CD4 T
VetBooks.ir cells. This binding, in conjunction with binding to the chemokine
receptor CXCR4 (CD184), is required for FIV to infect a cell. Most
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naturally infected cats suffer a critical loss of CD4 T cells. This loss
is due to destruction of infected cells, decreased production, and
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premature apoptosis (Fig. 40.5). The surviving CD4 cells may show
reduced responses to mitogens. FIV cats may show a shift away
from a Th1 cytokine production pattern. They may also show an

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increase in CD8 T cells. As a result, the CD4/CD8 ratio of FIV-
infected cats may drop to less than one. FIV chronically activates
Treg cells, which further contributes to the immunosuppressive
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effect by downregulating IL-2 production and inhibiting CD4 T cell
proliferation. Affected cats show decreased IL-2 and IL-12
production as well as increased IL-10. Thus the rise in the IL-10/IL-
12 ratio is especially immunosuppressive.

FIG. 40.5 The major immunosuppressive pathways activated in
feline immunodeficiency virus infections.

During the acute phase of FIV, Treg cells are infected and
activated by the virus. The virus induces both Foxp3 and

membrane-bound TGF-β production and as a result suppresses IL-2
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production by CD4 Th1 cells. The TGF-β converts Th1 cells into
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Treg cells. The Treg cells also suppress CD8 T cell responses by

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